Ferroptosis: An Energetic Villain of Age-Related Macular Degeneration

Iron homeostasis plays an important role in maintaining cellular homeostasis; however, excessive iron can promote the production of reactive oxygen species (ROS). Ferroptosis is iron-dependent programmed cell death that is characterized by excessive iron accumulation, elevated lipid peroxides, and t...

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Main Authors: Na Zhao, Siyu Li, Hao Wu, Dong Wei, Ning Pu, Kexin Wang, Yashuang Liu, Ye Tao, Zongming Song
Format: Article
Language:English
Published: MDPI AG 2025-04-01
Series:Biomedicines
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Online Access:https://www.mdpi.com/2227-9059/13/4/986
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author Na Zhao
Siyu Li
Hao Wu
Dong Wei
Ning Pu
Kexin Wang
Yashuang Liu
Ye Tao
Zongming Song
author_facet Na Zhao
Siyu Li
Hao Wu
Dong Wei
Ning Pu
Kexin Wang
Yashuang Liu
Ye Tao
Zongming Song
author_sort Na Zhao
collection DOAJ
description Iron homeostasis plays an important role in maintaining cellular homeostasis; however, excessive iron can promote the production of reactive oxygen species (ROS). Ferroptosis is iron-dependent programmed cell death that is characterized by excessive iron accumulation, elevated lipid peroxides, and the overproduction of ROS. The maintenance of iron homeostasis is contingent upon the activity of the transferrin receptor (TfR), ferritin (Ft), and ferroportin (FPn). In the retina, iron accumulation and lipid peroxidation can contribute to the development of age-related macular degeneration (AMD). This phenomenon can be explained by the occurrence of the Fenton reaction, in which the interaction between divalent iron and hydrogen peroxide leads to the generation of highly reactive hydroxyl radicals. The hydroxyl radicals exhibit a propensity to attack proteins, lipids, nucleic acids, and carbohydrates, thereby instigating oxidative damage and promoting lipid peroxidation. Ultimately, these processes culminate in cell death and retinal degeneration. In this context, a comprehensive understanding of the exact mechanisms underlying ferroptosis may hold significant importance for developing therapeutic interventions. This review summarizes recent findings on iron metabolism, cellular ferroptosis, and lipid metabolism in the aging retina. We also introduce developments in the therapeutic strategies using iron chelating agents. Further refinements of these knowledges would deepen our comprehension of the pathophysiology of AMD and advance the clinical management of degenerative retinopathy. A comprehensive search strategy was employed to identify relevant studies on the role of ferroptosis in AMD. We performed systematic searches of the PubMed and Web of Science electronic databases from inception to the current date. The keywords used in the search included “ferroptosis”, “AMD”, “age-related macular degeneration”, “iron metabolism”, “oxidative stress”, and “ferroptosis pathways”. Peer-reviewed articles, including original research, reviews, meta-analyses, and clinical studies, were included in this paper, with a focus on the molecular mechanisms of ferroptosis in AMDs. Studies not directly related to ferroptosis, iron metabolism, or oxidative stress in the context of AMD were excluded. Furthermore, articles that lacked sufficient data or were not peer-reviewed (e.g., conference abstracts, editorials, or opinion pieces) were not considered.
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spelling doaj-art-a584c1d21e664a27a9bfb4c15cd2b4822025-08-20T02:17:19ZengMDPI AGBiomedicines2227-90592025-04-0113498610.3390/biomedicines13040986Ferroptosis: An Energetic Villain of Age-Related Macular DegenerationNa Zhao0Siyu Li1Hao Wu2Dong Wei3Ning Pu4Kexin Wang5Yashuang Liu6Ye Tao7Zongming Song8Henan Eye Institute, Henan Eye Hospital, People’s Hospital of Zhengzhou University, Henan University School of Medicine, Henan Provincial People’s Hospital, Zhengzhou 450003, ChinaCollege of Medicine, Zhengzhou University, Zhengzhou 450001, ChinaCollege of Medicine, Zhengzhou University, Zhengzhou 450001, ChinaCollege of Medicine, Zhengzhou University, Zhengzhou 450001, ChinaCollege of Medicine, Zhengzhou University, Zhengzhou 450001, ChinaHenan Eye Institute, Henan Eye Hospital, People’s Hospital of Zhengzhou University, Henan University School of Medicine, Henan Provincial People’s Hospital, Zhengzhou 450003, ChinaHenan Eye Institute, Henan Eye Hospital, People’s Hospital of Zhengzhou University, Henan University School of Medicine, Henan Provincial People’s Hospital, Zhengzhou 450003, ChinaHenan Eye Institute, Henan Eye Hospital, People’s Hospital of Zhengzhou University, Henan University School of Medicine, Henan Provincial People’s Hospital, Zhengzhou 450003, ChinaHenan Eye Institute, Henan Eye Hospital, People’s Hospital of Zhengzhou University, Henan University School of Medicine, Henan Provincial People’s Hospital, Zhengzhou 450003, ChinaIron homeostasis plays an important role in maintaining cellular homeostasis; however, excessive iron can promote the production of reactive oxygen species (ROS). Ferroptosis is iron-dependent programmed cell death that is characterized by excessive iron accumulation, elevated lipid peroxides, and the overproduction of ROS. The maintenance of iron homeostasis is contingent upon the activity of the transferrin receptor (TfR), ferritin (Ft), and ferroportin (FPn). In the retina, iron accumulation and lipid peroxidation can contribute to the development of age-related macular degeneration (AMD). This phenomenon can be explained by the occurrence of the Fenton reaction, in which the interaction between divalent iron and hydrogen peroxide leads to the generation of highly reactive hydroxyl radicals. The hydroxyl radicals exhibit a propensity to attack proteins, lipids, nucleic acids, and carbohydrates, thereby instigating oxidative damage and promoting lipid peroxidation. Ultimately, these processes culminate in cell death and retinal degeneration. In this context, a comprehensive understanding of the exact mechanisms underlying ferroptosis may hold significant importance for developing therapeutic interventions. This review summarizes recent findings on iron metabolism, cellular ferroptosis, and lipid metabolism in the aging retina. We also introduce developments in the therapeutic strategies using iron chelating agents. Further refinements of these knowledges would deepen our comprehension of the pathophysiology of AMD and advance the clinical management of degenerative retinopathy. A comprehensive search strategy was employed to identify relevant studies on the role of ferroptosis in AMD. We performed systematic searches of the PubMed and Web of Science electronic databases from inception to the current date. The keywords used in the search included “ferroptosis”, “AMD”, “age-related macular degeneration”, “iron metabolism”, “oxidative stress”, and “ferroptosis pathways”. Peer-reviewed articles, including original research, reviews, meta-analyses, and clinical studies, were included in this paper, with a focus on the molecular mechanisms of ferroptosis in AMDs. Studies not directly related to ferroptosis, iron metabolism, or oxidative stress in the context of AMD were excluded. Furthermore, articles that lacked sufficient data or were not peer-reviewed (e.g., conference abstracts, editorials, or opinion pieces) were not considered.https://www.mdpi.com/2227-9059/13/4/986age-related macular degenerationironlipid peroxidationferroptosis
spellingShingle Na Zhao
Siyu Li
Hao Wu
Dong Wei
Ning Pu
Kexin Wang
Yashuang Liu
Ye Tao
Zongming Song
Ferroptosis: An Energetic Villain of Age-Related Macular Degeneration
Biomedicines
age-related macular degeneration
iron
lipid peroxidation
ferroptosis
title Ferroptosis: An Energetic Villain of Age-Related Macular Degeneration
title_full Ferroptosis: An Energetic Villain of Age-Related Macular Degeneration
title_fullStr Ferroptosis: An Energetic Villain of Age-Related Macular Degeneration
title_full_unstemmed Ferroptosis: An Energetic Villain of Age-Related Macular Degeneration
title_short Ferroptosis: An Energetic Villain of Age-Related Macular Degeneration
title_sort ferroptosis an energetic villain of age related macular degeneration
topic age-related macular degeneration
iron
lipid peroxidation
ferroptosis
url https://www.mdpi.com/2227-9059/13/4/986
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